Significance The basal forebrain (BF) is traditionally recognized as a brain structure crucial for arousal, attention, learning, and memory. Here, we discovered a causal role of the BF in the control of prosocial behavior, which is fundamental for our daily life. We showed in mice that the BF somatostatin-expressing inhibitory neurons predominantly target GABA neurons and disinhibit dopamine neurons in the ventral tegmental area and thereby increase dopamine release in the nucleus accumbens. This disinhibitory circuitry played an essential role in promoting social interaction behavior. Our findings identify a previously unknown function of the BF in social behavior regulation and suggest a potential therapeutic target for social deficits commonly observed in major neuropsychiatric disorders.